When sleeping or resting in non-supine positions, normal forces are distributed over areas of the face and head in contact with a surface, such as a mattress or arm. For many non-supine positions this path is through at least one eye. The resulting load may cause deformation, stress, strain, and or damage to the eye, eye orbit, and or its surrounding anatomy. Yet another problematic effect of a load path passing through the eye area is shifting in the position of prescription orthokeratology (ortho-k) lenses prescribed for reshaping the cornea. That is, when forces are distributed over areas of the face and head in contact with a surface, with the load path through at least one eye, the force causes deformation of the eye and displacement or shifting of the lens. Such lens shift can negatively impact the effectiveness of corneal correction and often results in prolonged blurring of vision. This problem may be magnified when the lenses are worn throughout the night.
Ortho-k lens wearers who encounter shifting of lens position receive the challenging and impractical guidance of restricting sleep to supine (or avoid sleeping in non-supine) positions—e.g., lying on the back or having the face upward. A fundamental problem with guidance to avoid sleeping in non-supine positions is that many people are non-supine or side sleepers and will not be comfortable or be able to sleep in only a supine position. Moreover, merely shielding, covering, or surrounding the eye area with protection, without load-bearing structure that provides an alternative path bypassing the eye and surrounding soft tissues, will not adequately disperse loads introduced by sleeping or resting in non-supine positions. Thus, improper or superficial protections may not be able to prevent deformation, stress, strain, and or damage to the eye. Additionally, deformation, stress, and strain to the eye and surrounding tissue may inhibit the eye's ability to regulate intraocular pressure by contributing to sustained elevation of episcleral venous pressure, orbital venous pressure, trabecular meshwork outflow resistance, and or choroidal expansion. Impairment of the eye's ability to self-regulate intraocular pressure would in turn exacerbate symptoms of glaucoma, other eye diseases, or eye damage.
Pressure within the eye, or intraocular pressure (IOP), arises from a balance of the inflow of aqueous humor from ciliary secretion processes and outflow of aqueous humor through tissues such as the trabecular meshwork, as well as the magnitude of episcleral venous pressure. These three are balanced to provide sufficient pressure within the eye (typically IOPs of 10-21 mm Hg above atmospheric pressure) so that the eye globe remains inflated. This balance has been quantitatively defined by Goldman in the 1950's as: IOP=F/C+EVP, where F is aqueous humor inflow, C is the outflow facility, EVP is episcleral venous pressure and IOP is the intraocular pressure. Elevation of episcleral venous pressure when in a horizontal position has been associated with an increase in nighttime intraocular pressure. Additional increases in episcleral venous pressure and or a decrease in aqueous outflow associated with loads on the eye, eye orbit, and surrounding anatomy due to sleep position would contribute to an additional increase in the intraocular pressure. An increase in orbital venous pressure due to sleep position induced loads could also contribute to an increase in outflow resistance and disrupt the intraocular pressure self-regulation process needed for return of intraocular pressure back to normal healthy levels. Expansion of the choroid circumference or thickness due to sleep position related deformation, stress or strain of the eye could also contribute to an increase in outflow resistance and further disrupt the ability of the eye to self-regulate intraocular pressure and an elevation in intraocular pressure. In summary, there are a variety of mechanisms whereby loads on the eye could produce an increase episcleral venous pressure and or a decrease aqueous outflow and a disruption of the ability to self-regulate IOP, causing IOP to increase.
A well-established method for lowering IOP levels utilizes the Honan Intraocular Pressure Reducer, a pre-surgical device which compresses the eye and is used specifically to lower IOP and thereby reduce the risk of explosive vitreous loss upon incision. The Honan Intraocular Pressure Reducer works by applying a compressive pressure of between 20 and 30 mm Hg to the eye. This external pressure causes an increase in the rate of fluidic outflow through the trabecular meshwork relative to the rate of fluid inflow, without affecting the episcleral venous pressure and thereby lowering the internal eye pressure, i.e. lowering IOP. See Peter J. McDonnell, The Honan Intraocular Pressure Reducer, 103 Archives of Opthalmology 422, 422-425 (1985); James El Morgan et al., Intraocular Pressure After Peribulbar Anaesthesia: Is the Honan Balloon Necessary?, 79 British Journal of Opthalmology 46, 46-49 (1995).
There is a distinction between the direct application of pressure to the eye produced by this common pre-surgical practice, which applies pressure directly to the eye and eyelid, and the deformation, stress and strain of the eye, eye orbit, and its surrounding anatomy introduced by the loads on the eye associated with side- and face-down sleep positions. Sleep-position related forces can raise episcleral and orbital venous pressure, increasing trabecular meshwork outflow resistance along with choroidal expansion, all of which may contribute to sustained IOP elevation due to impairment of the ability of the eye to self-regulate back to normal healthy levels. Such sustained IOP increase, over and above the known increase in IOP associated with being in a horizontal position, could contribute to serious eye damage including but not limited to glaucomatous eye damage and deformation.
Normal IOP levels are in the range of 10-21 mm Hg. Normal IOP levels vary somewhat according to the time of day, usually being higher in the morning than later in the day. IOP levels of at least ˜10 mm Hg are needed for the eye globe to retain its shape. Tonometry is used to measure IOP indirectly from observation of cornea surface deflections in response to a known force. Currently, IOP cannot be measured while a person is sleeping, although sensors that can be used for this are under development—e.g., Sensimed's Triggerfish® sensors. Factors generally considered and or known to be correlated with the manifestation of glaucoma include low blood pressure, high blood pressure, thin corneal walls, and low blood supply to the optic nerve as well as a number of other physiological considerations and bio-chemical considerations. Generally, the first course of treatment for glaucoma patients includes eye drops to lower IOP to normal levels—e.g., prostaglandins in conjunction with beta blockers.
Glaucoma is an eye disorder where the optic nerve suffers damage and retinal ganglion cells die. Glaucoma permanently impacts vision, progressing to blindness if left untreated and is one of the leading causes of blindness worldwide. The cause of glaucoma is not known. Optic nerve damage due to glaucoma is often associated with an increase in intraocular pressure (IOP) to pressures above 21 mm Hg. However, some glaucoma patients with optic nerve damage do not exhibit elevated IOP levels. This type of glaucoma is sometimes called normal-tension or low-tension glaucoma. Several recent studies suggest IOP-related stress, strain, strain rates etc. of optic nerve head tissues contribute to glaucomatous cell damage. See Claude F. Burgoyne et al., The Optic nerve head as a Biomechanical Structure: A New Paradigm for Understanding the Role of IOP-Related Stress and Strain in the Pathophysiology of Glaucomatous Optic nerve Head Damage, 24 Progress in Retinal and eye Research 39, 39-73 (2005); Ian A. Sigal et al., Predicted Extension, Compression and Shearing of Optic Nerve Head Tissues, 85 Experimental Eye Research 313, 31-322 (2007); Ian A. Sigal et al., Biomechanics of the Optic Nerve Head, 88 Experimental Eye Research 799, 799-807(2009); Michael D. Roberts et al., Correlation between Local Stress and Strain and Lamina Cribosa Connective Tissue Volume Fraction in Normal Monkey Eyes, 51 Investigative Ophthalmology & Visual Science 295, 295-307 (2010); Barry Quill et al., The Effect of Graded Cyclic Stretching on Extracellular Matrix-Related Gene Expression Profiles in cultured Primary Human Lamina Cribrosa Cells, 52 Investigative Ophthalmology & Visual Science 1908, 1908-15 (2011); Richard E. Norman et al., Finite Element Modeling of the Human Sclera: Influence on Optic Nerve Head Biomechanics and Connections with Glaucoma, 93 Experimental Eye Research 4, 4-12 (2011).
Non-degenerative and degenerative eye damage may be reflected by load bearing pressure on the eye(s). For example, a person lying on a traditional mattress experiences pressures on the eye due to the weight of the head being uniformly distributed over the side of the face in contact with the mattress. The weight of the head is supported by the portion of the face resting on the mattress, and this portion of the face bears the resulting reaction force. The reaction force on the face is equal but in opposite direction to the weight of the head as: N=mg, where m is the mass of the head, and g is the gravitational constant, ˜9.81 Newtons/kg. The reaction force N in this example represents the force applied by the mattress against the head that prevents it from sinking through the surface. In many non-supine positions, the area of the face that rests on a surface includes at least one eye. Transmission of this force N or load through the eye area results in forces on tissues.
To illustrate the forces acting on the eye in these common positions, the following values for weight and surface area are employed. These values are approximations utilized to establish a force balance model of pressure exerted on the eye and actual values may vary from individual to individual. Assuming that the approximate average value for a human head weight is 10.0 pounds (lbs), it is estimated that the surface area in contact with a surface while resting or sleeping on the side will be rectangular in shape with dimensions of roughly 6.5 inches by 8.0 inches, with a surface area of 52.00 square inches. In this scenario, the weight of the head resting on the side of the face produces an average pressure (force per area) over the surface of the side of the face of 10 pounds per 52 square inches. This is equivalent to an average pressure of ˜0.19 pounds per square inch (psi) or ˜9.9 mm Hg. Newton's third law states that for every force there is a reaction force, equal in magnitude and acting in the opposite direction. This law is applied to estimate the increase in intraocular pressure due to the weight of the head pressing the eye against a surface during sleep. The human eye as a sphere with an approximate radius of 0.47 inch (12.0 mm) and thus a surface area of 2.8 in2. Assuming that when sleeping or resting approximately one third of the surface area of the eye is in contact with a surface that is exposed to a pressure of 0.19 psi, the pressure acts on the eye over a surface area of 0.93 in2, producing forces of 0.18 lb dispersed over the 2.8 in2 of the eye surface area. It is estimated, for purpose of this example, that this would cause an increase in intraocular of 0.065 psi or 3.3 mm Hg for the non-supine, side sleep or rest scenario. Given that the Honan pressure reducer is operated so as to apply a pressure of 20-30 mm Hg to the eye for periods of 5-30 minutes without causing damage to the eye, this 3 mmHg increment in IOP produced by the a pressure of ˜10 mm Hg from the weight of the head should be readily accommodated by a self-regulatory increase in aqueous outflow.
Various devices, goggles, eye-glasses and protective eye-gear are known in the art. For example, U.S. Pat. No. 6,155,261 to Day discloses a device that purports to assist with relieving elevation of IOP during sleep. U.S. Pat. No. 5,213,241 to Dewar et al. discloses a device that is used to protect the eye during physical activity. Sleep masks such as U.S. Pat. No. 5,343,561 to Adamo and other eye shield devices such as U.S. Pat. No. 5,183,059 to Leonardi appear to position a covering across the bony orbital rim of the wearer's eye but do not appear to absorb and or distribute normal forces exerted by a surface through a load path which bypasses the eye and surrounding tissue. However, none of these provide the necessary force distribution, force alleviation, and deformation avoidance attributes required to mitigate or prevent deformation, stress, strain, and or damage.